1. Intra-abdominal Hypertension: Emerging concept in AKI
Georg Auzinger
Honorary Senior Lecturer
Liver ICU & ECMO Lead
King’s College Hospital
London

2. The 4 compartments ICS TCS Plus a few more: Ocular Cardiac Hepatic
Renal
Pelvic
ACS
ECS

3. Background Concept of IAH/ACS known for > a century
Rediscovered only ~30 years ago…
despite the obvious!
CCM survey 2006:
25% of paediatric Intensivists never saw a case of IAH/ACS
24% were unaware of measurement methods
33% would never use decompressive laparotomy to treat ACS

4. Definition APP (Abdominal perfusion pressure): MAP - IAP
IAP: Steady state pressure within abdominal cavity
What is normal – it depends: ICU 5-7mmHg?
IAH: Sustained or repeat elevation of IAP ≥12mmHg
Paeds: IAP>10mmHg
ACS: Sustained IAP>20mmHg associated with new organ dysfunction/failure Fietsam R, et al. Am Surg 1989; 55:396–402
Paeds ACS reported at IAP>17mmHg or >10 if associated with OD
APP (Abdominal perfusion pressure): MAP - IAP

5. IAH Grading Grade I: IAP 12-15mmHg Grade II: IAP 16-20mmHg
Grade III: IAP 21-25mmHg
Grade IV: IAP>25mmHg

6. ACS Definition Primary Secondary Recurrent
Injury or disease of abdomen/pelvis – frequently requires surgery or radiological intervention
Secondary
Conditions not originating from abdomino-pelvic compartment
Recurrent
Syndrome redevelops after initial surgical or medical treatment of primary or secondary ACS

7. Incidence De Waele JJ, et al. Am J Kidney Dis
Incidence De Waele JJ, et al. Am J Kidney Dis. 2011;57: Thabet FC, et al. J Intensive Care Med. 2015: 1-6
IAH %
ACS %
Major abdominal surgery NA
33-41
Liver Transplant 31
Major Trauma 50
13-36
ICU
30-54
5-12
Septic shock
51-76 33
Severe acute pancreatitis
59-84
25-56
Paediatric patients
13%*
1-10%
*Increased abdominal wall compliance?

8. Pathogenesis Monro-Kellie doctrine Extrapolate to the abdomen…
Pressure volume relationship of structures within rigid cranial vault
Extrapolate to the abdomen…
Cranium
Abdomen
Organ(s)
Brain
Liver, Spleen, Gut
Fluid
CSF
Ascites
Enclosing structure
Skull
Abdominal cage
Lesion
Tumor, Blood
Blood, Air, Oedema, Tumor, Ascites
Pressure
ICP
IAP
Perfusion
CPP (60-70)
APP (>60)*
Rigid -
kind of
Rigid
*APP >50 predicts survival better than MAP and IAP
Cheatham ML, et al. J Trauma 2000;49: 621–626

9. But…
Elasticity of abdominal wall and diaphragm
Expressed as ΔP/ΔV

10. Aetiology (not exhaustive)
Increased intra-abdominal volume
Luminal: Gastroparesis, ileus, volvulus, colonic pseudo-obstruction
Solid organ: Hepato- and/or Splenomegaly
Mass lesions
Fluid: Ascites, Haemoperitoneum
Air: Intra and extraluminal
Decreased abdominal wall compliance
Emergency surgery/Damage control – tight closure
Abdominal wall bleeding/oedema/rectus sheath haematoma
Juxta-abdominal process affecting IAP
Surgical correction: Large hernia, gastroschisis, omphalozele
Combination of the above
Fluid shifts/capillary leak – Severe sepsis or septic shock
Massive fluid resuscitation
Burns eschars/sepsis
Severe necrotising pancreatitis
Complicated intra-abdominal infection

11. Liver trauma – intra-abdominal haemorrhage, Packing

12. SNP abdominal decompression

13. ALF - capillary leak, reperfusion injury - intestinal + abdominal wall oedema

14. Polycompartmental hypertension
Air (tension)
Air
Retroperitoneal bleed

15. There is rarely just one cause

16. Cont intragastric monitoring
How do we diagnose
Clinical assessment – physical examination inaccurate: Sensitivity 60% PPV 45-75%
“IAP should be expressed in mmHg and measured at end-expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line.”
CiMon
Cont intragastric monitoring
Goldstandard
Fluid volume important
Detrusor contraction
<25ml, or 1ml/kg Paeds
Bias of -4.9mmHg vs
direct measurement
IAP≥20 – PPV 0, NPV 0.91

17. Imaging IVC narrowing Thickening enhancement of bowel wall
Reduced caliber of abdominal aorta
Displacement/compression of kidney(s)
Relative increase in AP vs transverse abdominal diameter

18. Pathophysiology
Abviser™

19. Pathophysiology in relation to AKI
IAH reduces renal arterial blood flow
IAH increases IVC pressure
IAH compresses renal vein – Renal vein pressure (RVP)↑
ACS increases RAP + reduces gradient for venous return
Oliguria at IAP of 15mmHg
Anuria at IAP of 25mmHg
Thresholds lower in hypovolaemic states or sepsis

20. Pathophysiology RPP (Renal perfusion pressure): MAP – RVP
RFG (Renal filtration gradient): Glomerular filtration pressure – proximal tubular pressure = RPP – RVP = MAP – 2 x RVP
In case of IAH: RVP = IAP RFG: MAP – 2 x IAP
Bradley SE. J Clin Invest 1947;26: 1010–1022 – IAP induced ↑RVP led to sig drop in GFR, RPF and UOP

21. Other factors Increased intra-capsular/parenchymal pressure
ACS induced reduction in CO: ↑Afterload ↓Preload
ACS induced Catecholamine, Aldosterone, Renin and Angiotensin release
Impaired intestinal perfusion: Bacterial translocation, cytokine release with deleterious effects on renal perfusion

22. Treatment of IAH/ACS

23. Treatment

24. Summary IAP, IAH, ACS only fairly recently “re-discovered”
Understanding of its importance under appreciated
Paediatric ICU practice lagging behind?
Syndrome with potentially devastating consequences
ACS in many studies one of the most important outcome predictors
IAH/ACS is frequently a poly-compartmental disease
Warrants a high index of suspicion
Low threshold for monitoring – should be regularly repeated
Early intervention
Whenever possible via least invasive approach PCD > surgery
Less frequently a surgical disease today

25. Summary Kidneys are a primary target organ during IAH/ACS
AKI occurs very early, initially often subclinical
Prime importance of RVP and RPP
The IVCP and RAP are important and often neglected parameters
As with many other syndromes: Paradigm of early aggressive fluid resuscitation followed by timely restrictive fluid management
Aim to reduce IVCP and RVP
In our hands RRT and UF is an early interventional cornerstone